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Theresa Mau
e-mail address: tmau@umich.edu

Mentor: Raymond Yung, MB, ChB

Research Description

The World Health Organization estimates that at least 2.8 million people die each year as a result of being overweight (BMI ≥ 25) or obese (BMI ≥ 30). Obesity has long been associated to many diseases, especially type 2 diabetes (44%), cardiovascular disease (23%), and certain cancers (7-41%). When it was discovered that obesity itself induces a chronic, low-grade, metabolic inflammation state, a plethora of research interest has begun to steer towards the investigation of the role and function of inflammation in obesity, termed metaflammation. Growing evidence reveals that aside from individual lifestyle choices, the development of obesity can also be attributed to genetic disposition, particularly epigenetic processes. In 1992, Hales and Barker were the first to propose the “thrifty phenotype hypothesis” which highlights the association between low birth weight and an observed increase in late life disease risk due to the fetus making adaptations (e.g. insulin resistance) to survive maternal malnourishment. This leads the fetus into generating an adaptive phenotype that would have to eventually cope with a different postnatal environment. Much of the immune system is developed in utero and is therefore potentially susceptible to the influence of prenatal environmental factors. Others have shown that a prenatal diet rich in methyl-donors can alter the susceptibility to immune-mediated diseases such as reactive airway disease and inflammatory bowel disease in mouse models. Although this is thought to be secondary to the diet’s effect on DNA methylation, there is intriguing new data suggesting that prenatal micronutrients can also influence the health outcome of the F1 generation through alternation of the gut microbiome. The Yung lab has previously shown that maternal micronutrient (methyl donor diet) supplementation results in F1 C57/Bl/6 mice that are smaller in size (through 24 months of age) and have suppressed T cell chemokine receptors (CCR5, CCR2, and CXCR3) expression and function. Following this, a separate study in our lab showed that this prenatal diet can protect the F1 generation of ApoE -/- mice against atherosclerosis. The Yung lab has also recently found that age-related obesity is associated with increased adipose tissue macrophage (ATM) M1 phenotype and increased adipose tissue ER stress response. We hypothesize that a prenatal diet rich in methyl donors (MS diet) will protect the F1 generation from the development of obesity and obesity-associated inflammation by reducing M1 macrophage-mediated inflammation and adipose tissue ER stress response.




EM-PACE (Ethiopia-Michigan Platform for Advancing Collaborative Engagement) Grant, 2014

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